Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of the instillation of glucose, fat, casein hydrolysate, and HCl into the gastrointestinal tract upon plasma levels of somatostatin-like immunoreactivity (SLI) in the venous effluent of the pancreas, fundus and antrum of the stomach, and in the inferior vena cava (IVC) were determined in normal laparotomized dogs. Fasting SLI levels in the effluent plasma from these sites were significantly greater than IVC levels. The intragastric administration of glucose elicited a prompt and significant rise in SLI levels in pancreatic, fundic and antral venous plasma, and in IVC plasma; intraduodenal glucose elicited smaller increments. After intragastric fat, a smaller, more gradual increase in the pancreatic and fundic effluents was observed, whereas the rise in antral SLI was minute, and IVC SLI did not rise significantly. Intraduodenal fat elicited a prompt increase in the pancreatic and antral vein SLI levels, and a small but significant increase in fundic and IVC plasma which suggests faster release of enteric factors that influence SLI secretion in the pancreas and antrum. Intragastric casein hydrolysate elicited a prompt increase in SLI in both the pancreatic and fundic veins, the latter being marked, but the antral SLI response was small; IVC SLI rose significantly within 15 min. Intragastric HCl provoked a prompt and marked rise in pancreaticoduodenal and antral vein SLI but no increase in fundic vein SLI; IVC SLI levels rose significantly within 20 min. Intraduodenal HCl elicited an even more prompt and marked pancreatic SLI response, and SLI rose significantly in both the fundic and antral venous effluents; IVC SLI also rose more promptly. In dogs with a gastric fistula that prevented intraduodenal entry of HCl, intragastric HCl elicited only a very small and transient rise in pancreaticoduodenal vein SLI, markedly stimulated the antral SLI response, but completely suppressed fundic venous SLI levels. The results indicate that all three nutrients stimulate SLI release from the pancreas and stomach. The greater SLI response to intragastric, as opposed to intraduodenal, glucose suggests that unidentified local factors are of importance. The responses to the intraduodenal instillation of HCl and fat suggest a role of enteric hormones in the release of SLI from the pancreas and fundus and antrum of the stomach. Additionally, there is evidence of direct effects of HCl upon gastric SLI release.
J Clin Invest 1978 Sep
PMID:Pancreatic and gastric somatostatin release in response to intragastric and intraduodenal nutrients and HCl in the dog. 69 Jan 83

The aim of the present experiments was to determine the effects of basal glucagon on glucose production after induction of prolonged insulin lack in normal conscious dogs fasted overnight. A selective deficiency of insulin or a combined deficiency of both pancreatic hormones was created by infusing somatostatin alone or in combination with an intraportal replacement infusion of glucagon. Glucose production (GP) was measured by a primed constant infusion of [3H-3]glucose, and gluconeogenesis (GNG) was assessed by determining the conversion rate of circulating [14C]alanine and [14C]lactate into [14C]glucose. When insulin deficiency was induced in the presence of basal glucagon the latter hormone caused GP to double and then to decline so that after 4 h it had returned to the conrol rate. The conversion of alanine and lactate into glucose, on the other hand, increased throughout the period of insulin lack. Withdrawal of glucagon after GP had normalized resulted in a 40% fall in GP, a 37% decrease in GNG, and a marked decrease in the plasma glucose concentration. Induction of insulin deficiency in the absence of basal glucagon resulted in an initial (30%) drop in GP followed by a restoration of normal GP after 2--3 h and moderately enhanced glucose formation from alanine and lactate. It can be concluded that (a) the effect of relative hyperglucagonemia on GP is short-lived; (b) the waning of the effect of glucagon is attributable solely to a diminution of glycogenolysis because GNG remains stimulated; (c) basal glucagon markedly enhances the GNG stimulation apparent after induction of insulin deficiency; and (d) basal glucagon worsens the hyperglycemia pursuant on the induction of insulin deficiency both by triggering an initial overproduction of glucose and by maintaining the basal production rate thereafter.
J Clin Invest 1978 Sep
PMID:Effect of glucagon on glucose production during insulin deficiency in the dog. 69 Jan 90

Somatostatin, a growth hormone-release inhibiting hormone, has been found to be a powerful inhibitor of gastric and pancreatic secretion as well as of hormone release in the digestive system. This study was undertaken to determine the influence of somatostatin on the myoelectrical activity pattern of the small bowel. Three conscious dogs were prepared with electrodes spaced 25 cm apart along the entire small intestine. Intravenous infusions of somatostatin were administered in various doses (0.6--5.0 microgram/kg.h) while spike activity and slow waves were recorded under fasting conditions, after a meat meal, or during intravenous infusion of gastrin, caerulein, or insulin. Somatostatin at a dose of 0.6 microgram/kg.h almost doubled the frequency of the interdigestive myoelectric complex. Somatostatin in fed dogs caused a dose-dependent decrease of the normal fed spike activity, and at higher doses it induced a pattern like that seen in fasting animals. The slow-wave frequency in both fasted and fed conditions was not changed significantly. We conclude that somatostatin given under basal conditions increases the frequency of the interdigestive complex and, when administered after feeding, converts the fed-type pattern to the fasted-type pattern. It may therefore play a promoting role in initiating the interdigestive myoelectric complex.
Am J Physiol 1978 Sep
PMID:Effect of somatostatin on myoelectrical activity of small bowel. 69 18

At least four types of endocrine-like cells have been detected histochemically in the mucosa of the human colon and rectum, i.e. argentaffin cells storing 5-hydroxytryptamine (5HT) and non-argentaffin cells reacting with glucagon, somatostatin and bovine pancreatic peptide (BPP) antibodies. Ultrastructurally, four main types and three rare types of endocrine-like cells have been identified. Among the former cells were: (1) argentaffin EC1 cells, known to store 5HT and substance P, (2) poorly argyrophil L cells, corresponding to the glucagon-immunoreactive cells storing enteroglucagon or glucagon-like immunoreactivity (GLl), (3) inconstantly argyrophil F-like cells, possibly corresponding to BPP-immunoreactive cells, and (4) fairly argyrophil H cells of unknown function. Rare D cells, corresponding to somatostatin cells, N cells, corresponding to neurotensin cells, and P cells, of unknown function, have been also found.
Cell Tissue Res 1978 Sep 05
PMID:Types of endocrine cells in the human colon and rectum. 69 14

The interaction between motilin and somatostatin on gastrointestinal motor activity was studied in fasted, unanesthetized dogs. Contractions of the stomach, duodenum, jejunum, and ileum were recorded with extraluminal strain gage force transducers. Motilin initiated a pattern of contractile activity which closely resembled phase III of the interdigestive motor complex. Somatostatin delayed the onset of the motilin response and reduced motor activity in the stomach and the jejunum. During somatstatin infusion the motilin-induced contractile pattern did not migrate to the jejunum. The cycle of natural interdigestive motor complexes was also interrupted by somatostatin. Somatostatin alters natural and motilin-induced interdigestive migrating motor complexes of the canine gastrointestinal tract.
Am J Dig Dis 1978 Sep
PMID:Somatostatin inhibits motilin-induced interdigestive contractile activity in the dog. 70 49

Somatostatin and Des(Ala1Gly2)desaminol[Cys3]descarboxy-]Cys14[-]D-Trp8[dicarba3,14-somatostatin (Ia) are more potent inhibitors of glucagon, insulin and growth hormone release than the L-Trp8 analog (Ib). However when infused intravenously, these three compounds are equipotent but short-acting inhibitors of pentagastrin evoked gastric secretion in the dog. The duration of inhibition of equieffective antisecretory doses is significantly increased following subcutaneous administration 30 min prior to a food stimulus. The longest duration of antisecretory action is seen with the D-Trp8 analog (Ia) after subcutaneous administration.
Arch Int Pharmacodyn Ther 1978 Sep
PMID:Subcutaneous administration of somatostatin analogs as a major factor in the enhancement of the duration of action. 73 88

These experiments were designed to determine whether brain lesions which elevate nonstress plasma levels of GH and disrupt stress-induced suppression of GH secretion in female rats affect the median eminence content of somatostatin. Some rats received lesions in the medial or lateral preoptic-anterior hypothalamic area (PO-AHA), while others received anterior hypothalamic cuts. Sham-operated and intact rats served as controls. GH and somatostatin were measured by RIA. Medial but not lateral PO-AHA lesions caused elevated nonstress plasma GH levels at 2, 14, 17, and 23 weeks after surgery, but normal levels were obtained at autopsy at 27 weeks. These lesions compromised GH responses to stress at 14 and 23 weeks. Rats with anterior hypothalamic cuts showed elevated nonstress GH levels at 17, 23, and 27 weeks after surgery and loss of the GH response to stress at 14 and 23 weeks. Median eminence content of somatostatin was reduced approximately 80% in rats with medial PO-AHA lesions or anterior cuts. Whereas medial PO-AHA lesions were associated with normal body length and weight and evidence of estrogen secretion, anterior hypothalamic cuts produced increased linear growth and body weight and signs of functional castration. These results suggest that the effects of lesions which cause prolonged elevation of nonstress GH levels and disruption of the GH stress response are due to interference with somatostatin neurons located in the medial PO-AHA. Somatostatin content of the median eminence seems to depend largely on connections originating in or traversing the medial PO-AHA.
Endocrinology 1978 Sep
PMID:Somatostatin content of the median eminence in female rats with lesion-induced disruption of the inhibitory control of growth hormone secretion. 74 18

Somatostatin (1 mug/ml) inhibited glucose (16.7 mM)-stimulated 45Ca uptake by isolated rat islets incubated in media containing no added calcium or calcium at a low concentration (0.2mM). Epinephrine (50 mug/ml) and mannoheptulose (20mM) also inhibited 45Ca uptake by islets incubated in the presence of calcium (0.2mM). Addition of glucose (16.7 mM) caused a small but significant increase in insulin release from islets incubated in media containing no added calcium. In the presence of a low concentration of calcium (0.2 mM), glucose caused a much greater increase in insulin secretion which was inhibited by addition of somatostatin, epinephrine or mannoheptulose.
Endocrinology 1976 Sep
PMID:Inhibition of calcium uptake by somatostatin in isolated rat islets of Langerhans. 78 58

Somatostatin, insulin and glucagon were localized in the principal islets of the anglerfish (Lophius americanus) and the channel catfish (Ictalurus punctata) by means of the unlabeled antibody-peroxidase-antiperoxidase immunocytochemical method. Both species showed a similar ratio of positive cells 9:6:4 (insulin:somatostatin:glucagon), but the interrelations of the three cell types differed between species. The large number of somatostatin-positive cells may be indicative of an important role for this hormone in teleost physiology. The principal islets appear to be a good source of tissue for further work on somatostatin.
Am J Anat 1976 Sep
PMID:Immunohistochemical localization of somatostatin, insulin and glucagon in the principal islets of the anglerfish (Lophius americanus) and the channel catfish (Ictalurus punctata) (1) (2). 78 93

Equine pancreas was investigated with immunohistochemical methods to study the distribution of endocrine cells immunoreactive to anti-insulin, anti-glucagon, and anti-somatostatin. A-cells demonstrable by anti-glucagon are located in the center of Langerhans islets and frequently in the duct epithelium. Few A-cells are seen associated to acini. Anti-insulin reactive B-cells form a large zone around the center of the Langerhans islets in which some B-cells lie between exocrine cells and others, although few, are located in the duct epithelium. D-cells stained with anti-somatostatin serum form a discontinuous outermost zone around the Langerhans islets. In some islets the D-cells are also observed among the B-cells or between the border of A- and B-cells. Single D-cells are seen in the duct epithelium or between acinar cells. In younger horses, endocrine cells are more frequently associated in bulges of the duct system. The histotopographic relation between these endocrine cell types is discussed with respect to its functional significance.
Cell Tissue Res 1976 Sep 29
PMID:Insulin-, glucagon-, and somatostatin-immunoreactive endocrine cells in the equine pancreas. 79 97


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